V 20TH ANNIVERSARY
5 May 1999
CE Refereed Peer Review
FOCAL POINT
★Regardless of the mechanistic
origin, the importance of
supraventricular tachycardia
(SVT) is its ability to cause
hemodynamic compromise,
which can result in clinical
manifestations of cardiac disease.
KEY FACTS
■ SVT can result from disorders
in impulse formation, impulse
conduction, or a combination
of both.
■ Narrow QRS complexes and P
waves are generally present with
SVT; but P waves may be difficult
to identify, especially if they are
superimposed on the QRS or T
waves.
■ Although many SVTs cannot be
eliminated by medical or surgical
intervention, therapy may
decrease the hemodynamic
consequences of the arrhythmia
and improve the patient’s health.
■ Digoxin is the drug of choice for
many SVTs, but β-adrenergic and
calcium-channel blockers are
also used.
Vol. 21, No.
Overview of
Supraventricular
Tachycardia in Dogs
and Cats
The Ohio State University
Tamara Grubb, DVM, MS
William W. Muir III, DVM, PhD
ABSTRACT: Supraventicular tachycardia (SVT) is one of the most common arrhythmias in
dogs and cats. The clinical mechanisms for SVT are divided into three categories of disorders:
impulse formation, impulse conduction, or a combination of the two. The electrocardiographic
characterization of SVT varies slightly with the anatomic origin of atrial activation but generally
is characterized by a detectable P wave and normal QRS configuration and duration. Regard-
less of the cause, the importance of SVT is directly related to its hemodynamic consequences.
Therapeutic urgency depends on the severity of hemodynamic compromise, clinical signs, and
presence and significance of concurrent heart disease.
S
upraventricular tachycardia (SVT) is among the most common arrhyth-
mias in dogs1–13 and cats.14–19 Supraventricular (SV) arrhythmias, which are
any arrhythmias that originate in or require atrial or atrioventricular (AV)
junctional tissue as part of the electric circuit,20,21 are referred to as supraventricular
tachycardia when the heart rate (HR) is faster than 140 beats/min in giant-breed
dogs, 160 beats/min in medium-sized dogs, 180 beats/min in toy-breed dogs,
220 beats/min in puppies, and 240 beats/min in cats.22–24 Common clinical caus-
es for SVT (see Causes of Supraventricular Tachycardia) include pain, fear, exer-
cise, abnormal autonomic tone, pyrexia, acid–base and electrolyte disorders, en-
docrine abnormalities, and primary cardiac disease. Cardiac diseases associated
with SVT include chronic AV valvular insufficiency,10,22,23,25 congenital heart de-
fects,9,11,16 dilated cardiomyopathy (DCM),6,13 and hypertrophic cardiomyopathy
(HCM).19
Regardless of the cause, the importance of SVT is directly related to its hemo-
dynamic consequences. Clinical signs are a manifestation of altered hemody-
namics and range from mild (lethargy, exercise intolerance)4–6,9,13,17 to severe
(seizures, collapse), the latter of which can result in sudden death.7,8,10,18 Therapy
is designed to improve hemodynamic function and may be targeted at eliminat-
ing the arrhythmia or controlling the ventricular rate to optimize cardiac output
(CO) and blood flow.
Compendium May 1999 20TH ANNIVERSARY
MECHANISMS OF CARDIAC ARRHYTHMIAS
Ultimately, the fundamental causes for all cardiac ar-
rhythmias can be traced to derangements in either the
active or passive electrophysiologic properties of the
heart. Active properties are those associated with the
transmembrane flux of ions, particularly sodium, potas-
sium, and calcium. Passive properties are those deter-
mined by the various structural elements (i.e., cell type,
cell size, spatial orientation) of the heart and their sub-
sequent inherent electric properties (ability to conduct
an electric pulse). Alterations in either the active or pas-
sive electric properties of the heart can be caused by
both physiologic (e.g., temperature, autonomic tone,
circulating neurohormones) and pathophysiologic (e.g.,
hypoxia, ischemia, acid–base and electrolyte imbal-
ances) processes.
Clinically, the mechanisms for SVT are divided into
three principal categories: disorders of impulse forma-
tion, disorders of impulse conduction, and a combina-
tion of the two. Impulse formation or automaticity
(i.e., spontaneous rate of discharge) is generally most
rapid in the sinoatrial (SA) node, which is the natural
Causes of Supraventricular Tachycardia
■ Noncardiac (clinical)
— Miscellaneous (pain, fear, excitement,
hypothermia, pyrexia, hypovolemia, hypoxia,
trauma, shock, sepsis, neoplasia)
— Autonomic imbalance (increased sympathetic
tone, decreased parasympathetic tone)
— Acid–base and electrolyte imbalance (acidosis,
alkalosis, hyperkalemia, hypokalemia,
hypercalemia, hypocalcemia, hypomagnesemia)
— Endocrinopathy (hypothyroidism,
hyperthyroidism, Addison’s disease,
pheochromocytoma)
— Drug toxicity (digitalis, sedative drugs [e.g.,
xylazine], medetomidine, opioids, anesthetic
agents [e.g., ketamine, halothane], catecholamines
[e.g., epinephrine], dopamine, antiarrhythmic
agents [e.g., lidocaine, quinidine], bronchodilators
[e.g., terbutaline])
— Organic disease (gastrointestinal, respiratory,
renal, hepatic, central nervous system)
AV = atrioventricular; DCM = dilated cardiomyopathy; HCM = hypertrophic cardiomyopathy.
ACTIVE AND PASSIVE PROPERTIES ■ IMPULSE FORMATION AND CONDUCTION
Small Animal/Exotics
pacemaker in normal hearts. Although the AV node,
His’ bundle, and some Purkinje fibers have the proper-
ty of automaticity, they are considered subsidiary pace-
makers because their inherent rate of discharge is slower
than that of the SA node. Disorders of impulse forma-
tion include abnormal sinus automaticity, abnormal au-
tomaticity in pacemakers that are normally subsidiary,
automaticity in tissues that are generally not automatic,
and the onset of triggered impulses. Potential causes of
abnormal automaticity are stretch, hypoxia, electrolyte
imbalances, or inflammatory disease. Triggered impuls-
es occur when premature electric impulses arise during
the early (early afterdepolarization) or late (delayed af-
terdepolarization) phase of repolarization. Because early
and delayed afterdepolarizations are premature (i.e., oc-
cur before the next normal impulse), they spread
through tissues that have not fully repolarized and are
still partly refractory and lead to disorders of impulse
conduction.
Disorders of impulse conduction include altered im-
pulse transmission as a result of physiologic mechanisms
(e.g., autonomic imbalance), pathologic mechanisms
— Mechanical stimulation (pacemaker implantation, cardiac
catheterization, placement of central venous catheter)
■ Cardiac
— Arrhythmia (cardiac disease or condition)
— Atrial tachycardia (chronic AV valvular
disease,1,11, 22–25 mitral valve defects,48 tricuspid
dysplasia,45 HCM in cats47)
— Atrial fibrillation or flutter (chronic or degenerative
AV valvular insufficiency,22–25,43,46 congenital mitral
insufficiency,44,48 tricuspid valvular hypoplasia or
dysplasia,44,50 valvular endocarditis,1,44
DCM,5,6,13,43,46,49 HCM in cats,17,19,43 patent ductus
arteriosus,44 pulmonary stenosis,3,44 subaortic
stenosis,44 double-chambered right ventricle44)
— Accessory pathways (tricuspid dysplasia in dogs and
cats,9,16 DCM,6 HCM in cats,17 five-chambered heart9)
— Junctional and AV nodal tachycardia (chronic AV
valvular disease,1,22,23 sick sinus syndrome,10
myocarditis1)
Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

(e.g., myocardial ischemia,

hypoxia, inflammation), and
anatomic anomalies (e.g.,
bypass tracts, accessory path-
ways). Impulse transmis-
sion from one area of the
heart to another may be
slowed and potentially
blocked or may follow ab-
normal pathways during A B
these conduction distur-
bances. During a phenome-
non called reentry, slowed
antegrade (forward) con-
duction results in retro-
grade (backward) activa-
tion of myocardial tissue
that is in disparate phases
of repolarization, resulting
in chaotic transmission of
circuit impulses. Reentry, C D
or circus activity, is the me-
Figure 1—Electrocardiographic tracing of (A) P waves buried within T waves. P waves begin to
chanism for many SVTs, emerge, and the heart rate (HR) is 210 beats/min. (B) The arrhythmia can be definitively diag-
including atrial fibrillation
nosed as supraventricular tachycardia (SVT) as the HR is slowed (190 beats/min) and P waves
and flutter. begin to emerge. QRS complexes are inverted in this patient. (C) Inverted P waves (P’ ) are char-
acteristic of junctional tachycardia. (D) SVTs with wide QRS complexes can be confused with
DIAGNOSIS ventricular arrhythmias. Note the P waves that occur for every QRS complex and the normal PR
Electrocardiography interval, allowing a definitive diagnosis of SVT with aberrant ventricular conduction. The HR is 240
The electrocardiographic beats/min. (Tracings A, B, and D, paper speed = 25 mm/sec; tracing C, paper speed = 50 mm/sec)
(ECG) characterization of
SVTs (Figure 1) varies
slightly with the anatomic origin of atrial activation but lead II generally indicate impulse origination from an
is generally characterized by a detectable P wave and ectopic pacemaker in the atrium, as occurs in atrial
normal QRS configuration and duration.20 In dogs and tachycardia (AT).22,26 P waves have various shapes in
cats, P waves generated in lead II are usually easy to multifocal AT because the impulse originates at multi-
identify and are typically used for quantitative and ple sites.20,26 P waves are inverted in the standard limb
qualitative evaluations.22 P waves are also generally easy leads during retrograde stimulation of the atria, as often
to identifiy in the precordial chest leads (CV 5RL, occurs in junctional tachycardia.10,22 Junctional tachy-
CV6LL, CV6LU, and V10).22 However, ECG complexes cardia can also occur with no P waves. P waves are ab-
(P, QRS, and T waves) may be absent in any lead when sent in atrial standstill and sinus arrest and are un-
the surface electric activity is perpendicular (isoelectric) identifiable during atrial fibrillation and flutter.3–5,19
to the lead or in any lead with very low voltage. Thus, The PR interval of an impulse initiated in the SA
all leads should be evaluated for the presence of a P node can vary but should be of normal duration. The
wave. PR interval following an impulse initiated at a site oth-
Superimposition of P waves with the QRS complex, er than the SA node is generally prolonged because
ST segment, or T wave can make identification of P conduction to the AV node does not proceed rapidly
waves difficult during tachycardia.7,12,22,23 Slowing of the along the specialized atrial conduction pathways. 20
HR by vagal manipulation often enables the P waves to Conversely, the PR interval may be markedly shortened
emerge from the other complexes, allowing identifica- if an accessory pathway connects the atria directly to
tion of P-wave morphology. A normal upright (posi- the AV junction or ventricular myocardium.20 In the
tive) and rounded P wave and normal PR interval in most common type of accessory pathway SVT (Wolff-
lead II indicate that the impulse likely originated in the Parkinson-White syndrome), the QRS duration is pro-
SA node.22 Positive but abnormally shaped P waves in longed with early activation of but delayed conduction

P-WAVE MORPHOLOGY ■ ATRIAL TACHYCARDIA ■ JUNCTIONAL TACHYCARDIA

Compendium May 1999 20TH ANNIVERSARY Small Animal/Exotics

through the ventricular TABLE I of the dive reflex are tech-

muscle, resulting in an early, Anticipated Response of Supraventricular niques commonly used in
slurred upstroke of the ini- Tachycardia to Vagal Stimulation42 human medicine to physio-
tial portion of the QRS logically enhance vagal tone
Type Response
complex (delta wave).9,12,16,18 and slow the HR.20 These
In all other SVTs without Sinus tachycardia Gradual and transient techniques, however, are im-
concurrent aberrant conduc- slowing of or no change in practical in veterinary medi-
heart rate
tion anomalies, the QRS 22 cine. Vagal stimulation is
Atrial tachycardia Rapidly terminated or no
duration is not prolonged 42
effect or increased atrial performed by gradually in-
and SVTs are commonly rate with slowing and creasing pressure to one or
classified as narrow complex regulation of ventricular both carotid arteries or to
tachycardias. QRS complex- rate25 each eyeball for 10 to 30
es may not occur with every Atrial flutter Temporary slowing of heart seconds (Figure 2).27,28 The
P wave (second-degree AV rate, transformation into results of this maneuver are
block) if the SV rate is too atrial fibrillation or no more consistent in hu-
rapid for all impulses to be effect mans20,21 than in animals.27
conducted through the AV Atrial fibrillation Temporary slowing of heart Pharmacologic manipula-
rate or no effect
node to the ventricles.22,28 Atrioventricular nodal Cessation of tachycardia or
tion of the AV node is more
tachycardia no effect successful and includes ad-
Physiologic and ministration of calcium-
Accessory pathway Cessation of tachycardia or
Pharmacologic no effect channel blockers (e.g.,
Maneuvers Junctional tachycardia Temporary slowing or diltiazem and verapamil),
Physiologic and pharma- cessation of tachycardia β-adrenergic blockers (e.g.,
cologic maneuvers that alter propranolol and esmolol),
the generation and conduc- morphine, adenosine, and
tion of cardiac electric im- edrophonium sulfate, all of
pulses in the SA and AV which can prolong AV con-
nodes can be used to slow duction and create tempo-
ventricular rate, thereby rary AV node block.20,32
helping to differentiate the Intravenous (IV) dilti-
anatomic site of SVT origin. azem, a rapid-acting calci-
SVTs can occasionally be um-channel blocker, and
abolished by augmented va- esmolol, a rapid-acting β-
gal tone because many auto- adrenergic blocker, can be
matic arrhythmias depend Figure 2A administered cautiously and
on high sympathetic tone are currently the most com-
for maintenance and reen- mon pharmacologic agents
trant arrhythmias often de- used for diagnosis and emer-
pend on rapid conduction gency treatment of SVT in
through the AV node.27 Re- veterinary medicine. 29–31
sponse to vagal stimulation Adenosine, a rapid-acting
may be temporary, but any endogenous nucleotide, is
response can be important popular as emergency thera-
in obtaining a diagnosis and py for SVT in humans; but
may be crucial in emergency its efficacy in dogs and cats
situations. Vagal stimula- is not well documented. 27
tion, however, does not in- Figure 2B Edrophonium, an anticho-
variably slow the HR in pa- Figure 2—Examples of enhancing vagal tone by using (A) oc- linesterase, increases acetyl-
tients with heart failure or ular pressure and (B) carotid body massage. choline concentration at the
high sympathetic tone. 27 neuromuscular junction,
Table I lists the anticipated response of tachycardias to thereby decreasing the HR. The use of edrophonium,
physiologic and pharmacologic manipulation. however, is limited because side effects can occur from
Deep breathing, Valsalva’s maneuvers, and initiation accumulation of acetylcholine in other tissues (e.g., in-

VAGAL STIMULATION ■ PHARMACOLOGIC MANIPULATION ■ INTRAVENOUS BLOCKERS

Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

Figure 3A Figure 3B Figure 3C

Figure 3—Electrocardiographic tracing of (A) normal sinus complexes (first three and last one, single solid arrow), a fusion com-
plex (fourth, open arrow), and complexes initiated in the left ventricle (fifth and sixth, double solid arrows). Note that the QRS
complexes of the ventricular beats are inverted (indicating initiation in the left ventricle), extremely wide, and abnormal in ap-
pearance and that the large T wave is opposite in polarity to the QRS complex. Tracings of (B) a premature ventricular complex
initiated in the right ventricle (single solid arrow). (C) Ventricular tachycardia initiated in the right ventricle. The first complexes
are initiated at the sinus node. Note that the QRS complexes of the ventricular beats are upright (indicating initiation in the right
ventricle), extremely wide, and abnormal in appearance and that the large T wave is opposite in polarity to the QRS complex.
(paper speed = 25 mm/sec)

creased production of respiratory secretions, gastroin- to physiologic or pharmacologic manipulation of vagal

testinal hypermotility).
DIFFERENTIATION BETWEEN
SUPRAVENTRICULAR AND
VENTRICULAR TACHYCARDIA
Determining whether an arrhythmia is SVT or ven-
tricular tachycardia (VT) affects the choice of therapy,
therapeutic urgency, and prognosis. SVT can be differ-
entiated from VT by evaluating the QRS complexes
(Figure 3). VT is characterized by wide, bizarre QRS
complexes that are often of large amplitude. Because of
this ECG feature, VT is often called wide-complex
tachycardia. QRS complexes during VT can be negative
or positive, and T waves are generally opposite in polar-
ity to the QRS deflection. QRS complexes that are neg-
ative in lead II are considered to be of left ventricular
origin and those that are positive of right ventricular
origin. The latter may be difficult to differentiate from
SVT with concurrent conduction disturbances (e.g.,
left or right bundle branch block).
Tachycardia with normal-appearing P waves that are
not associated with a QRS complex (AV dissociation) is
diagnostic for VT. This is in contrast to second-degree
AV block, which occurs with very rapid SVTs.22,28 Very
rapid HRs, however, can make recognition of P waves
difficult. ECGs recorded for extended periods (2 to 5
minutes) facilitate the recognition of P waves as they
emerge from the previous T wave. Vagal maneuvers
(e.g., ocular pressure, carotid body massage) or the use
of drugs that alter autonomic tone (e.g., diltiazem, es-
molol) can be administered to slow the HR and facili-
tate a diagnosis. Most SVTs respond, at least transiently,
tone; whereas VTs generally do not respond. Other
ECG characteristics of VTs include the presence of fu-
sion or capture beats.23
HEMODYNAMIC CONSEQUENCES
Regardless of the electrophysiologic mechanisms or
cause, the importance of AT or VT is directly related to
the hemodynamic consequences. Generally, the hemo-
dynamic consequences of cardiac arrhythmias can be
linked to four key factors: the ventricular rate, timing
of atrial relative to ventricular contraction, pattern of
ventricular activation, and presence of underlying car-
diovascular disease or other diseases that impair tissue
perfusion. Tissue perfusion ultimately depends on
maintaining adequate CO, which is the product of the
HR and stroke volume (i.e., the amount of blood eject-
ed from the heart with each beat).
Heart rates that are extremely slow (40 beats/min or
slower in dogs; 60 beats/min or slower in cats) cause an
obvious decrease in CO. HRs that are extremely rapid
can cause an increase in CO until a critical rate is
reached (180 beats/min or faster in dogs; the critical
rate for cats is unknown) (Figure 4),28 beyond which
ventricular filling is impaired (thus decreasing the
stroke volume) and diastolic duration is decreased. Be-
cause the myocardium receives most of its blood supply
during diastole when the myocardium is relaxed, short-
ened diastole can lead to decreased myocardial perfu-
sion. Extremely rapid HRs also impose substantial
metabolic demand on the heart. Increased oxygen (O2)
demand (rapid HR) with impaired O2 delivery (de-
creased perfusion) can result in cardiac ischemia, heart

WIDE-COMPLEX TACHYCARDIA ■ AV DISSOCIATION ■ KEY HEMODYNAMIC FACTORS

Compendium May 1999 20TH ANNIVERSARY Small Animal/Exotics

failure, or both. In fact, rapid car- reported in dogs.34 Sudden death in

diac pacing is one of the more ef- cats is suggested to be caused by
fective experimental methods used SVTs associated with HCM. 35
to reduce CO and produce heart Seizures and behavioral changes in
failure in dogs.33 dogs have been linked to hypoxic
Loss of coupling of atrial to ven- lesions in the brain, assumed to
tricular contractions and ATs or have occurred during arrhythmia-
VTs that occur prematurely can re- induced cerebral ischemia.36 SVT
sult in inadequate ventricular filling can cause myocardial ischemia re-
and reduction of stroke volume. sulting from decreased tissue perfu-
Hemodynamics can also be im- sion and O2 delivery subsequent to
paired if rhythm disturbances cause impaired diastolic filling during
abnormal and ineffective patterns rapid HRs. This can lead to further
of ventricular activation. This is fre- myocardial damage and heart fail-
quently observed during rapid or ure. Indeed, impaired perfusion
accelerating polymorphic or multi- can cause hypoxia, metabolic
form ATs or VTs (e.g., fibrilla- changes, and resultant clinical
tion).27 Underlying cardiac or other manifestations in virtually all or-
disease that limits the force of ven- gans and tissues.
tricular contraction and reduces
CO will further impair tissue perfu- THERAPY
sion, impede the success of therapy, General Considerations
and result in a less favorable prog- The urgency of treating SVT de-
nosis. pends on the severity of hemody-
namic compromise, clinical signs,
Figure 4— Electrocardiographic (top) and
CLINICAL SIGNS and presence and significance of con-
blood pressure (bottom) tracings obtained
Clinical signs (see Clinical Signs from a direct arterial line. Note the dimin- current heart disease. Therapy may
Associated with Supraventicular ished blood pressure when the atrial rate is not be required for paroxysmal (in-
Tachycardia) are almost always a increased to 300 beats/min (solid arrows). termittent) SVT without hemody-
manifestation of altered hemody- (aVf = lead; AoP = aortic pressure) namic compromise in patients with-
namics and vary considerably. Short out heart disease.22,27,28 Conversely,
durations of paroxysmal tachycar- SVT causing rapid sustained (contin-
dia of SA nodal origin may go unnoticed because of the uous) ventricular rates may lead to acute deterioration of
absence of significant hemodynamic effects. However, hemodynamic function; thus, immediate and effective
rapid sustained SVTs that eliminate the atrial contribu- therapy is often crucial. Therapeutic plans should be de-
tion to cardiac filling and produce a rapid ventricular vised to reduce ventricular rate, even if the SVT is refrac-
rate that exceeds the critical tory to treatment. Some
HR can result in drastically SVTs cannot be eliminated,
Clinical Signs Associated with
decreased CO, thereby causing but therapy may decrease the
severe hemodynamic compro- Supraventricular Tachycardia severity and improve the pa-
mise. tient’s health. Not all SVTs
Common clinical signs or Lethargy Ataxia should be treated and not all
consequences of hemody- Exercise intolerance Syncope antiarrhythmic drugs are be-
namic compromise include Coughing Seizures nign. In some instances,
lethargy, exercise intoler- Weakness Sudden death treatment may actually exac-
ance, weakness, ataxia, syn- erbate the SVT (e.g., digital-
Pulmonary edema (associated with SVT-induced
cope, seizures, signs of sys- is-induced AV block) or
temic congestion (e.g., ascites, left-sided heart failure) cause decompensation of the
peripheral edema), signs of Systemic edema and ascites (associated with SVT- cardiovascular system (e.g.,
pulmonary congestion (e.g., induced right-sided heart failure) negative inotropic effects of
dyspnea, coughing), and sud- β-adrenergic and calcium-
den death. Sudden death SVT = supraventricular tachycardia. channel blockers).22,27,28,36,37
precipitated by ATs has been Drug choice is based on

COMMON SIGNS ■ MYOCARDIAL ISCHEMIA ■ TREATMENT ALTERNATIVES

Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

TABLE II
Common Drugs for Treating Arrhythmiasa

Drug Type of Arrhythmia Clinical Effect Side Effects

Digitalis Atrial tachycardia; Slows conduction of AV node; AV block; AV junctional rhythm;

glycosides atrial fibrillation; increases parasympathetic tone; atrial or ventricular ectopic
(e.g., digoxin) atrial flutter; any improves cardiac contractility beats; ventricular tachycardia;
with concurrent anorexia; vomiting; diarrhea;
heart failure lethargy; ataxia
β-adrenergic All types of SVT; Inhibits sympathetic input to Decreased cardiac contractility;
blockers (e.g., digitalis-induced SVTs; the heart; decreases conduction sinus arrest; bradycardia; AV
propranolol, SVT secondary to WPW and automaticity block; hypotension; lethargy;
esmolol) bronchoconstriction;
hypoglycemia
Calcium-channel All types of SVT; Slows sinus node rate; Sinus arrest; AV block;
blockers (e.g., rapid ventricular prolongs refractory period sinus bradycardia; sinus block;
diltiazem, response to SVTs of AV node hypotension; lethargy; syncope;
verapamil) constipation; urinary retention
Procainamide SVTs secondary to WPW; Prolongs atrial and ventricular Decreased cardiac contractility;
occasionally used for refractory period; slows hypotension; AV block;
SVTs that are refractory electric conduction; widened QRS complex;
to other therapy depresses automaticity; has multiform ventricular tachycardia;
indirect vagolytic effects weakness; anorexia;
vomiting; diarrhea; fever;
leukopenia
Quinidine Acute atrial fibrillation; Prolongs atrial and ventricular Same as for procainamide
occasionally used for SVTs refractory period; depresses
that are refractory to other automaticity
therapy
Lidocaine Occasionally used for SVTs Depresses automaticity Increased AV conduction during
that are secondary to WPW (primarily in ventricular atrial flutter/fibrillation;
cells) hypotension; seizures;
tremors; excitation; emesis
Phenytoin Arrhythmias caused by Depresses diastolic AV block; dermatoses;
digitalis toxicity depolarization and ataxia; tremors; depression;
automaticity; counteracts toxic in cats
depression of AV nodal
conduction
Amiodarone or Refractory SVTs; SVTs Slows sinus node rate; Pulmonary fibrosis; thyroid
bretylium secondary to WPW prolongs AV node refractory abnormalities; corneal
time; inhibits sympathetic deposits; vomiting
nervous system; prolongs
refractory periods of His-Purkinje
system and of anomalous
pathways (as in WPW)
Edrophonium Atrial tachycardia Increases vagal tone Bradycardia; hypotension;
excitation; seizures; dyspnea;
vomiting, diarrhea
Anticholinergics Junctional tachycardia Decreases vagal tone; allows Tachycardia; ventricular
(e.g., atropine, SA node to resume as arrhythmias; gastrointestinal
glycopyrrolate) primary pacemaker ileus; ocular drying; drying of
salivary and respiratory
secretions
a
Drugs are listed in descending order from most to less commonly used.
AV = atrioventricular; SVT = supraventricular tachycardia; WPW = Wolff-Parkinson-White syndrome.

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Small Animal/Exotics Compendium May 1999
therapeutic efficacy, occurrence of side effects and toxic-
ity, and interactions with other drugs. Effective therapy
for recalcitrant SVT or patients in heart failure often re-
quires several drugs. Treatment with multiple drugs may
increase the toxicity of one or all of the drugs by altering
the pharmacokinetics. Drug choice is also based on
available routes of administration and required dosing
intervals, which are designed for client compliance. For
example, the administration of extended-duration dilti-
azem36,38,39 requires once-daily oral dosing, which is easy
for most clients. Emergency IV therapy may be needed,
but oral administration is preferred for patients with sta-
ble hemodynamics and as long-term therapy.
If SVT is secondary to a known underlying cause,
appropriate steps should be taken to alleviate the cause
or correct the problem. Therapeutic approaches include
alleviation of pain, fear, hypoxia, hypercarbia, and ane-
mia or reestablishment of hydration and electrolyte and
acid–base balance. The pharmacologic treatment of
SVTs generally falls to a small group of drugs (Table II)
that are used to decrease the sinus rate, normalize SV
electric activity, or decrease AV nodal conduction and
subsequently the ventricular rate. The most common
therapeutic drugs with these activities are digitalis, β-
adrenergic blockers (e.g., propranolol), and calcium-
channel blockers (e.g., diltiazem). Occasionally, class I
antiarrhythmics (e.g., lidocaine), unconventional drugs
(e.g., amiodarone), or seemingly paradoxic drugs (e.g.,
anticholinergics) are needed for effective therapy.
Therapeutic Agents
Digitalis
Digitalis is the drug of choice for many SVTs, espe-
cially those caused by reentry. 22 Digitalis increases
parasympathetic tone to the SA and AV nodes, slows
conduction through atrial tissue and the AV node, and
improves myocardial contractility. Digitalis is the first
line of therapy for most patients in heart failure; but for
patients with adequate cardiac function, other thera-
peutic agents (primarily β-adrenergic and calcium-
channel blockers) may control the HR more effectively.
Because increased contractility may be detrimental to a
thickened heart muscle, digitalis is generally contraindi-
cated in patients with HCM, especially those with ven-
tricular outflow obstruction.32 Side effects include anor-
exia; vomiting; diarrhea; lethargy; and numerous
arrhythmias, including AV block, AV junctional rhythm,
atrial and ventricular ectopic beats, and VT. The potential
for digitalis toxicity is increased by hypokalemia and by
the concurrent use of other drugs, including the antiar-
rhythmic agents verapamil, quinidine, and amiodarone.
Although digitoxin is still available, digoxin is the form of
digitalis used almost exclusively in dogs and cats.
HEART FAILURE ■ ACTIONS OF DIGITALIS
Compendium May 1999 20TH ANNIVERSARY Small Animal/Exotics

β-Adrenergic Blockers decompensation and result in death.32 Verapamil is not

β-adrenergic blockers or antagonists (class II antiar-
rhythmic agents) decrease automaticity and slow con-
duction through the AV node, thereby decreasing the
ventricular response rate. Propranolol, a nonselective
(i.e., produces β1- and β2-receptor blockade) β-adrener-
gic antagonist, has been used extensively in dogs and
cats.22,25,27,28,32 However, the side effects from β2-receptor
blockade (primarily bronchoconstriction) make this
drug inappropriate for patients with asthma or small
airway disease.32 Individual responses to propranolol
vary considerably, and doses must be carefully titrated
to each patient.32 Propranolol is lipophilic and easily
crosses the blood–brain barrier and can cause central
recommended for patients in heart failure.22
Side effects include sinus arrest, AV block, hypoten-
sion, lethargy, and syncope but are uncommon when
diltiazem is used at therapeutic doses.32 Because of the
potential for marked decreases in HR and myocardial
contractility, β-adrenergic and calcium-channel block-
ers are not generally used simultaneously.32
Class I and Class III Antiarrhythmics
Class I antiarrhythmic agents (e.g., procainamide,
quinidine, phenytoin) have local anesthetic effects and
depress abnormal automat-
icity and conduction and in- ENDIU
MP

M’
20th

CO
nervous system (CNS) effects, including depression and crease refractoriness. These

S

disorientation.32 agents can produce pro- 1 9 7
9 - 1
9 9 9

ANNIVERSARY
Atenolol, a β1-selective antagonist, may become the found hypotension when
β-adrenergic blocker of choice for prolonged treatment IV administration is rapid.
of many SVTs in dogs because of the drug’s lack of β2-
receptor side effects and because once-daily oral dos-
Other side effects include
sinus arrest, AV block, VT
A LookBack
ing25,27,28 may improve client compliance. In addition, and fibrillation, negative An enigma exists as to whether
CNS side effects are absent because hydrophilic drugs inotropy, nausea, and con- our greatest achievement in
do not easily cross the blood–brain barrier. Esmolol, vulsions. Class III antiar- diagnosing and treating
another hydrophilic β1-selective antagonist, can be used rhythmic agents (e.g., amio- arrhythmias has evolved from
for emergency therapy or diagnosis of acute, hemody- darone and bretylium) the technologic or
namically unstable SVT; but its extremely short half- prolong myocardial refrac-
pharmacologic realm. Without
life makes this drug less ideal for long-term therapy.32 toriness and, although
technologic advances, namely
Other β-adrenergic blockers, including metoprolol, more often used to treat
nadolol, and sotalol, have been used successfully as an- VT, are occasionally used more sensitive
tiarrhythmic agents in dogs.32 Side effects include nega- to treat SVTs that are unre- electrocardiograms and more
tive inotropic effects (which can worsen congestive sponsive to other therapeu- accurate means of measuring
heart failure [CHF]), sinus arrest, AV block, hypoten- tic modalities. Side effects cardiac function, veterinarians
sion, bronchospasm, and lethargy. Patients should be include conduction distur- would not be able to diagnose
carefully evaluated for signs of heart failure before ther- bances, bradycardia, and arrhythmias consistently or
apy is initiated. If heart failure is present, digitalization pulmonary fibrosis. predict their consequences. On
before administration of these agents is recommended.32 the other hand, without the
Specific Considerations pharmacologic advances,
Calcium-Channel Blockers Paroxysmal SVT without veterinarians would not be in a
Calcium-channel blockers (class IV antiarrhythmics, hemodynamic compromise
position to offer clients a better
such as diltiazem and verapamil) inhibit calcium entry is generally not considered
prognosis for arrhythmias or
into cells, thereby suppressing the activity of calcium- an emergency and can be
dependent arrhythmias. The primary calcium-depen- treated with oral digitalis, their pets a better quality of life.
dent tissues in the heart are the SA and AV nodes. Thus diltiazem, propranolol, or
calcium-channel blockers can decrease the HR by de- atenolol. Patients in CHF
pressing sinus rate and slowing conduction through the are generally treated with
AV node. Diltiazem has a longer duration of action and digoxin and may require
a less negative inotropic effect than does verapamil and supportive therapy, such as
has thus become the calcium-channel blocker of choice diuretics (e.g., furosemide)
in dogs and cats.22,28,32 Sustained-release diltiazem can and O2 supplementation.27
be administered once every 24 hours,32,38,39 resulting in Infrequently, IV digoxin is
improved client compliance. Verapamil is a potent neg- used for emergency therapy and may be replaced by oral
ative inotrope and has some vasodilatory effects, a com- digoxin once hemodynamic stability has been achieved.
bination that can cause hypotension and cardiovascular If CHF is not present or for cats with HCM, β-adrener-

SIDE EFFECTS OF ANTIARRHYTHMICS ■ QUINIDINE ■ ELECTROCARDIOVERSION

Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

Considerations for Direct-Current Electrocardioversion sidered.22 Catheter ablation of accessory path-

of Supraventricular Tachycardia22 ways should be considered if accessory path-
way–mediated SVTs persist despite therapy.40,41
Indications ■ Ventricular fibrillation can
Complete ablation of the pathway will termi-
nate the SVT; and if heart failure has not de-
■ Symptomatic patients result if shock is delivered veloped, the patient generally will not require
with tachycardia that during the vulnerable further therapy.
is refractory to period (QT interval).
antiarrhythmic therapy ■ Synchronization is not CONCLUSIONS
required for defibrillation. Supraventricular tachycardia can be initiated
Mechanism by either the active (electrolyte flux) or passive
■ Synchronized discharge Contraindications (electric properties) components of the heart
of electric current during ■ Digitalis toxicity that when abnormal, lead to abnormalities in
ventricular depolarization ■ Hypokalemia electric impulse formation or conduction. P
waves are generally present during SVT and
(QRS complex) may ■ Severe mitral insufficiency
are associated with a QRS complex of normal
cause conversion of ■ Severe left atrial duration. This is in contrast to VT in which P
tachycardia to normal enlargement waves, if present, are dissociated from the wide
sinus rhythm. ■ Chronic atrial fibrillation QRS complexes. Occasionally, HRs are so
■ Atrial fibrillation or flutter rapid that the P wave is buried within the pre-
Considerations ceding T wave or QRS complex. In this case,
with concurrent
■ Discontinue digitalis. slowing of the HR should be attempted by ini-
atrioventricular block
■ Synchronize the tiating physiologic (e.g., ocular pressure) or
■ Sick sinus syndrome pharmacologic (e.g., esmolol) maneuvers that
cardioverter to the
■ A cardioverter that is not alter autonomic tone.
QRS complex.
synchronized with the The importance of SVT is related to its
■ Start cardioversion at low hemodynamic consequences and subsequent
QRS complex
setting (e.g., 25 J) and clinical signs, which range from mild (exercise
increase power as needed. intolerance, coughing) to severe (syncope), pos-
sibly resulting in sudden death. The goal of
gic or calcium-channel blockers are often considered for SVT therapy is to improve the hemodynamic
primary therapy. In the presence of CHF, both blockers status, either by eliminating the arrhythmia or slowing
are used with digoxin if digoxin alone fails to adequately the ventricular rate. Drugs commonly used to treat
control the HR or effectively improve hemodynamics. SVTs include digitalis, β-adrenergic blockers, and calci-
Some arrhythmias are best treated with more specific um-channel blockers. Quinidine, procainamide, and
therapy. For instance, quinidine is often used in an at- phenytoin have specific uses in the treatment of SVT.
tempt to convert acute-onset atrial fibrillation to nor- Occasionally novel drugs or physical intervention are re-
mal sinus rhythm; procainamide is often used to elimi- quired. However, clinicians should remember that not
nate impulse conduction over accessory pathways; and all SVTs require therapy and that antiarrhythmic drugs
phenytoin is specifically used to treat tachycardia caused by often produce proarrhythmic or negative inotropic side
digitalis toxicity. 27 effects that can worsen the patient’s condition.
Supraventricular tachycardia unresponsive to tradi-
tional therapy may require multiple-drug therapy, un- REFERENCES
conventional drugs (e.g., amiodarone), or physical in- 1. Patterson DF, Detweiler DK, Hubben K, Botts RP: Sponta-
neous abnormal cardiac arrhythmias and conduction distur-
tervention (i.e, electrocardioversion [electroshock] or bances in the dog: A clinical and pathological study of 3,000
catheter ablation). Electrocardioversion (see Considera- dogs. Am J Vet Res May:355–369, 1961.
tions for Direct-Current Electrocardioversion of 2. Tilley LP: Transtelephonic analysis of cardiac arrhythmias in
Supraventricular Tachycardia) is generally reserved for the dog—Diagnostic accuracy. Vet Clin North Am 13:395–
SVTs that are refractory to drugs in patients with clini- 408, 1983.
3. Riepe RD, Gompf RE: ECG of the month. JAVMA 202:
cal signs of heart failure. Underlying causes of SVT
374–376, 1993.
(e.g., digitalis toxicity, hypokalemia, anemia, pain) 4. de Madron E: ECG of the month. JAVMA 208:672–673, 1996.
should be eliminated before electrocardioversion is con- 5. French WB: ECG of the month. JAVMA 189: 654–655, 1986.
Compendium May 1999 20TH ANNIVERSARY
6. Miller MW, Bonagura JD, DiBartola SP: ECG of the month.
JAVMA 192:336–337, 1988.
7. Tidholm A: ECG of the month. JAVMA 184:154–155, 1984.
8. Drazner FH: ECG of the month. JAVMA 176:490–491, 1980.
9. Lamb WA, Snyder PS: ECG of the month. JAVMA
204:728–730, 1994.
10. Quagliariello RM, de Madron E: ECG of the month. JAVMA
197:60–61, 1990.
11. Sedlacek PL, Kittleson M, Olivier NB: ECG of the month.
JAVMA 188:816–817, 1986.
12. Atkins CE, Cali JV, Lombardo PS: ECG of the month.
JAVMA 205:983–984, 1994.
13. Hawe RS: ECG of the month. JAVMA 182:364–365, 1983.
14. Tilley LP, Liu SD, Gilbertson SR, Wagner BM, Lord PF:
Primary myocardial disease in the cat. Am J Pathol 86:493–
522, 1977.
15. Harpster NK: Cardiovascular diseases of the cat. Adv Vet Sci Comp
Med 21:39–74, 1977.
16. Meurs KM, Miller MW: ECG of the month. JAVMA 203:
649–650, 1993.
17. Goodwin JK: ECG of the month. JAVMA 197:854–855, 1990.
18. Berry CR, Lombard CW: ECG of the month. JAVMA 189:
1542–1543, 1986.
19. Robbins MA, Bright JM: ECG of the month. JAVMA 196:
1786–1787, 1990.
20. Wathan MS, Klein GJ, Yee R, Natale A: Classification and
terminology of supraventricular tachycardia. Card Clin 11:
109–119, 1993.
21. Ganz LI, Friedman PL: Supraventricular tachycardia. N Engl
J Med 332:162–173, 1995.
22. Tilley LP: Analysis of common canine and feline cardiac ar-
rhythmias, in Tilley LP (ed): Essentials of Canine and Feline
Electrocardiography: Interpretation and Treatment, ed 3.
Philadelphia, Lea & Febiger, 1992, pp 127–254.
23. Miller MS, Tilley LP: Electrocardiography, in Fox PR (ed):
Canine and Feline Cardiology. New York, Churchill Living-
stone, 1988, pp 43–90.
24. Hamlin RL: Heart rate of the cat. JAAHA 25:284–292, 1989.
25. Bonagura JD: Cardiovascular diseases, in Sherding RG (ed):
The Cat: Diseases and Clinical Management. New York,
Churchill Livingstone, 1994, pp 819–946.
26. Kastor JA: Multifocal atrial tachycardia. N Engl J Med 322:
1713–1717, 1990.
27. Bonagura JD, Muir WW: Antiarrhythmic therapy, in Tilley
LP (ed): Essentials of Canine and Feline Electrocardiography:
Interpretation and Treatment. Philadelphia, Lea & Febiger,
1992, pp 320–364.
28. Sisson DD: The clinical management of cardiac arrhythmias
in the dog and cat, in Fox PR (ed): Canine and Feline Cardi-
ology. New York, Churchill Livingstone, 1988, pp 289–308.
29. Dougherty AH, Jackman WM, Naccarelli GV, et al: Acute
conversion of paroxysmal supraventricular tachycardia with
intravenous diltiazem. Am J Cardiol 70:587–592, 1992.
30. Turlapaty P, Laddu A, Murthy S, et al: A titratable short-act-
ing intravenous beta blocker for acute critical care settings.
Am Heart J 114:866–885, 1987.
31. Shettigar UR, Toole JG, Appunn, DO: Combined use of es-
molol and digoxin in the acute treatment of atrial fibrillation
or flutter. Am Heart J 126:368–374, 1993.
32. Nelson RW, Couto CG (eds): Small Animal Internal Med-
icine. St. Louis, The CV Mosby Co, 1998, pp 69–93.
Small Animal/Exotics
33. Armstrong PW, Stopps TP, Ford SE, DeBold AJ: Rapid
ventricular pacing in the dog: Pathophysiologic studies of
heart failure. Circulation 74:1075–1084, 1986.
34. Beckett SD, Branch CE, Robertson BT: Syncopal attacks and
sudden death in dogs: Mechanisms and etiologies. JAAHA
14:378–383, 1978.
35. Liu SK, Tilley LP, Tashjian RJ: Lesions of the conduction
system in the cat with cardiomyopathy. Recent Adv Stud
Card Struc Metab 10:641–653, 1975.
36. Meierhenry EF, Liu SK: Atrioventricular bundle degenera-
tion associated with sudden death in the dog. JAVMA 172:
1418–1422, 1978.
37. Kittleson M, Keene B, Pion P, Woodfield J: Verapamil ad-
ministration for acute termination of supraventricular tachy-
cardia in dogs. JAVMA 193:1525–1529, 1988.
38. Johnson LM, Atkins CE, Keene BW, Bai SA: Pharmacokinetic
pharmacodynamic properties of conventional and CD-formu-
lated diltiazem in cats. J Vet Intern Med 10:316–320, 1996.
39. Maskasame C, Lankford S, Bai SA: The effects of chronic
oral diltiazem and cimetidine dosing on the pharmacokinetics
and negative dromotropic action of intravenous and oral dil-
tiazem in the dog. Biopharm Drug Dispos 13:521–537, 1992.
40. Wright KN, Atkins CE, Kanter R: Supraventricular tachy-
cardia in four young dogs. JAVMA 208:75–80, 1996.
41. Scherlag BJ, Wang X, Nakagawa J, et al: Radiofrequency ab-
lation of a concealed accessory pathway as treatment for in-
cessant supraventricular tachycardia in a dog. JAVMA 204:
1147–1152, 1993.
42. Wellens HJJ: The value of the ECG in the diagnosis of
supraventricular tachycardias. Eur Heart J 17:10–20, 1996.
43. Spaulding GL, Tilley LP: Atrial fibrillation in the dog and
cat. Proc AAHA 43:75–78, 1976.
44. Bohn FK, Patterson DF, Pyle RL: Atrial fibrillation in dogs.
Br Vet J 127:485–496, 1971.
45. deMadron E, Kadish A, Spear JF, Knight DF: Incessant atri-
al tachycardias in a dog with tricuspid dysplasia. J Vet Intern
Med 1:163–169, 1987.
46. Bonagura JD, Ware W: Atrial fibrillation in the dog: Clini-
cal findings in 81 cases. JAAHA 22:111–120, 1986.
47. Boyden PA, Tilley LP, Albala A, et al: Mechanisms for arte-
rial arrhythmias associated with cardiomyopathy: A study of
feline hearts with primary myocardial disease. Circulation 69:
1036–1047, 1984.
48. Liu SK, Tilley LP: Malformation of the canine mitral valve
complex. JAVMA 167:465–468, 1975.
49. Tilley LP, Liu SK: Cardiomyopathy in the dog. Recent Adv
Stud Cardiac Struct Metab 10:641–650, 1975.
50. Liu SK, Tilley LP: Dysplasia of the tricuspid valve in the dog
and cat. JAVMA 169:623–626, 1976.
About the Authors
Drs. Grubb and Muir are affiliated with the Department of
Veterinary Clinical Sciences, College of Veterinary
Medicine, The Ohio State University, Columbus, Ohio.
Both are Diplomates of the American College of Veteri-
nary Anesthesiologists, and Dr. Muir is also a Diplomate
of the American College of Veterinary Emergency and
Critical Care.